Abstract
Epstein-Barr virus (EBV) is typically found in a latent, asymptomatic state in immunocompetent individuals. Perturbations of the host immune system can stimulate viral reactivation. Furthermore, there are a myriad of EBV-associated illnesses including various cancers, post-transplant lymphoproliferative disease, and autoimmune conditions. A thorough understanding of this virus, and the interplay between stress and the immune system, is essential to establish effective treatment. This review will provide a summary of the interaction between both psychological and cellular stressors resulting in EBV reactivation. It will examine mechanisms by which EBV establishes and maintains latency and will conclude with a brief overview of treatments targeting EBV.
Highlights
Epstein-Barr virus (EBV), known as human herpesvirus 4, is a widely prevalent pathogen that infects 90% or more of the world population [1,2,3]
The integrated stress response (ISR) is a common cellular response to stressors that involves phosphorylating the eukaryotic translation initiation factor 2 alpha. eIF2α phosphorylation leads to a decrease in overall protein synthesis and an increase in the translation of certain genes involved in cell recovery and survival. eIF2α phosphorylation is mediated by the kinases heme-regulated eIF2α kinase (HRI), general control nonderepressible 2 (GCN2), PKR-like ER kinase (PERK), and double-stranded RNA-dependent protein kinase (PKR) [165]
This review explores how different types of stressors facilitate EBV reactivation
Summary
Epstein-Barr virus (EBV), known as human herpesvirus 4, is a widely prevalent pathogen that infects 90% or more of the world population [1,2,3]. Deleting gp220/350 did not completely abrogate EBV entry into numerous examined cell lines, including human B cells, lymphoid lines, and the majority of epithelial cell lines, infection was not as efficient in the absence of gp220/350. This indicates that gp220/350 is not necessarily required for infection of either epithelial or lymphocyte cell lines [41]. This review will begin with an overview of EBV reactivation and the lytic and latent cycles, including recent advances in our understanding of how EBV establishes and maintains latency. We will conclude with a brief overview of advances in treatments targeting EBV
Sign-in/Register to view highlights & summary 
Published Version (
Free)
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call